There are many documented pathophysiological and clinical effects of hypertension. These effects include the short-term effects resulting in poor health and bad work performance and the longer-term effects resulting in myocardial infarction, stroke, cardiac arrest, kidney disease, kidney failure and others. Moreover, the effects of hypertension may be exacerbated in conjunction with other diseases such as diabetes. In recent years it is estimated that more than 50% of deaths relating to cardiovascular disease in the United States alone was related to or resulted from hypertension. Hypertension remains the most common cause of cardiac failure or other disease states requiring some amount of hospitalization.
There has been significant and extensive research for treatment for hypertension. However, present treatments for such disorders are treatments such as administration of angiotensin converting enzyme inhibitors (ACE inhibitors). These treatments have serious shortcomings in long-term effectiveness, most notable the cost associated with these treatments and significant adverse effects.
There are also a vast number of publications with regard to the mechanisms of pathogenesis of hypertension. Extensive production and activity of angiotensin II is well accepted as one of the major sources in the development of hypertension, since its excess causes abnormally strong contraction of arteries, compromises process of arteries relaxation and lead therefore to elevated blood pressure. Thus, a massive effort is being undertaken to develop pharmaceutical compounds capable either to reduce formation of angiotensin II (i.e. ACE inhibitors which block a conversion of angiotensin I to angiotensin II by arterial wall cells) or to block a biological activity of angiotensin II (i.e. agonists of angiotensin receptors). Both classes of compounds are being tested in experimental conditions for their capacity to block angiotensin-dependent contraction of arterial wall either using arteries isolated from laboratory animals or a model of cultured smooth muscle cells embedded in collagen gel. A capacity of a tested compound to block a contractile activity of angiotensin II in such experimental models unequivocally means that this compound will block angiotensin II activity in in vivo conditions and will reduce angiotensin-driven hypertension.
Carini et al. describe procyanidins from grape seeds that enhance relaxation of human artery (Life Sci. Oct. 17, 2003; 73(22):2883–98). Shen et al. describe green tea catechins that evoke a phasic contraction in rat aorta, and Chen et al. describe purified green tea epicatechins on contraction. Sanae et al. describe the effects of catechins on vascular tone in rat thoracic aorta with endothelium. Huang et al. describe role of endothelium/nitric oxide in vascular response to flavonoids and epicatechin (Acta Pharmacol. Sin. Dec. 21, 2000(12): 1119–24). While these references suggest a possible role of green tea extracts in regulating vascular tone, its direct effect to smooth muscle cells is less clear. Little is know if other ingredients may enhance the effect of green tea extract on smooth muscle cell contraction.
In view of the foregoing, there is a need for a nutritional composition and method to directly inhibit smooth muscle cell contraction and hence treat the underlying hypertension disease. There is a need for a method of using such a nutritional composition to preserve and restore the sensitivity of the arteries to stimuli that would allow for proper contraction and relaxation of smooth muscle cells in the arteries.